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My Phase 2a > Endocrine Diseases > Flashcards

Endocrine Diseases Flashcards

1
Q

What is the aetiology of SIADH?

A
  • Tumours:small cell carcinoma of lung= most common. also Prostate, thymus, pancreas
  • Pulmonary lesions: pneumonia, TB
  • Metabolic causes: Alcohol withdrawal
  • CNS: Meningitis, tumours, head injury, subdural haematoma
  • Drugs: Chlorpromide, carbamezapine etc
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2
Q

Briefly explain the pathophysiology of SIADH?

A
  • Excess ADH release causes excess insertion of aquaporin 2 channels in apical membrane of collecting duct
  • Therefore excess water retention and hyponatraemia
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3
Q

How is SIADH diagnosed?

A
  • Low serum Na+, high urine Na+
  • Euvolaemia: normal blood vol
  • Low plasma osmolality, high urine osmolality
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4
Q

What are the signs + symptoms of SIADH?

A
  • Symptoms due to hyponatraemia
  • Varied and genetic
  • Anorexia, nausea and malaise
  • Weakness and aches
  • Reduction in GCS and confusion with drowsiness
  • Fits and coma if severe
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5
Q

How is SIADH treated?

A
  • Treat underlying cause
  • Restrict fluids to 500-1000ml daily
  • Hypertonic saline if really symptomatic to prevent brain swelling
  • Oral demeclocycline daily (Inhibits ADH)
  • Vasopressin antagonist [ADH antagonist] e.g. oral tovaptan daily
  • Salt and loop diuretic

Acute <48hrs = treat the hyponatraemia urgently to reduce risk of cerebral oedema
- Hypertonic saline 3%
Chronic >48hrs = slow and steady correction – max 10mmol/L/day
- Fluid restriction in mild to moderate cases
- ADH antagonists or demeclocycline in severe or symptomatic cases.

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6
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism= Excess production of aldosterone, independent of the renin-angiotensin system. Resulting in:
- increased sodium, and thus water retention
- increased blood pressure
- decreased renin release

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7
Q

What is the epidemiology of Conn’s syndrome?

A

Rare condition accounting for less than 1% of hypertension

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8
Q

What is the aetiology of Conn’s syndrome?

A
  • 2/3rds= Adrenal adenoma that secretes aldosterone
  • 1/3rd= Bilateral adeno-cortical hyperplasia
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9
Q

What are the risk factors for Conn’s syndrome?

A
  • Middle aged adults
  • Pts with family hx of early onset hypertension.
  • Conventional antihypertensives don’t work
  • Unusual symptoms e.g. sweating
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10
Q

Briefly explain the pathophysiology of Conn’s syndrome

A
  • Excess aldosterone production due to aldosterone producing carcinoma
  • Na+ and water retention, thus K+ loss (to balance charge
  • Thus hypokalemia and hypertension
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11
Q

What is the clinical presentation of Conn’s syndrome?

A
  • Often asymptomatic
  • Hypertension due to increased blood vol, associated with renal, cardiac and retinal damage
  • Hypokalaemia: Weakness, cramps, paraesthesia
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12
Q

How is Conn’s syndrome diagnosed?

A
  • U+Es: hypokalaemia + hypernatraemia
  • Plasma Aldosterone:Renin Ratio (ARR)= If increased aldosterone levels that are not suppressed w 0.9% saline infusion= Diagnostic
    • low renin + raised aldosterone = primary hyperaldosteronism
    • raised renin + raised aldosterone = secondary hyperaldosteronism
  • CT or MRI on adrenal
  • Hypokalaemic ECG= Flat T wave, ST depression, Long QT
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13
Q

How is Conn’s syndrome treated?

A
  • Laproscopic adrenalectomy
  • Aldosterone antagonist e.g. oral sprinolactone for 4 weeks pre-op to control BP and K+
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14
Q

What is gigantism?

A

Excessive GH production in children before fusion of the growth plates

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15
Q

What is acromegaly?

A

Excessive GH in adults

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16
Q

What is the aetiology of acromegaly?

A
  • Most cases are due to benign GH producing pituitary adenoma
  • rarely ectopic GH producing tumour e.g. pancreatic or lung tumours
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17
Q

What is the epidemiology of acromegaly?

A

Rare, increased incidence in middle age

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18
Q

What are the risk factors for acromegaly?

A

5% associated with MEN-1

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19
Q

Briefly explain the pathophysiology of acromegaly

A
  • Increased GH due to pituitary tumour or ectopic carcinoid tumour
  • Binds to receptors, resulting in increased IGF-1
  • This stimulates skeletal muscle and soft tissue growth
  • Local tumour expansion can also cause compression of the pituitary gland and bitemporal hemianopia
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20
Q

List some symptoms of acromegaly

A
  • Increased size of hands and feet
  • Prominent jaw
  • Headaches
  • Splayed teeth
  • Enlarged tongue
  • Excessive sweating
  • Bitemporal hemianopia
  • Snoring
  • Wonky bite
  • Weight gain
  • Low libido
  • irregular periods F and erectile dysfunction M
  • Backache
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21
Q

List some signs of acromegaly

A 
Skin darkening
Fatigue
Deep voice
Carpal tunnel syndrome
Macroglossia
Coarsening face with wide nose
Prognanthism and big supraorbital ridge
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22
Q

List some common co-morbidities with acromegaly

A
  • Diabetes
  • Sleep apnoea
  • CVS Problems
  • menstrual irregularities
  • erectile dysfunction
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23
Q

How is acromegaly diagnosed?

A
  • IGF1= Raised = Diagnostic
  • Glucose tolerance test= No suppression of GH= Diagnostic/ Gold standard
  • MRI of pituitary fossa
  • Old photos= See changes
  • Plasma GH levels= Can rule out acromegaly if random GH is undetectable or is low
  • Pituitary function test: high prolactin in20% of pts
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24
Q

How is acromegaly treated?

A
  • 1st line treatment= Trans-sphenoidal surgery to remove tumour and fix compression.
  • 2nd line = Dopamine agonist e.g. Oral cabergoline or somatostatin analogues e.g. IM octreotide
  • GH receptor antagonists if intolerant to SSA= Supresses IGF-1
  • Stereotactic radiotherapy
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25
Q

What is the epidemiology of diabetes mellitus type 1?

A

Typically occurs in childhood
Increasing incidence
Common in Northern Europe

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26
Q

Briefly explain the pathophysiology of T1DM

A
  • Absolute insulin deficiency caused by autoimmune destruction of the beta cells in the islets of Langerhans -> no insulin production + ↑ blood glucose
  • Low blood glucose -> glucagon secretion which tells the liver to convert glycogen into glucose via glycogenolysis.
    • the liver also converts lipids into glucose via gluconeogenesis
    • overall result is even more hyperglycaemia.
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27
Q

What is the aetiology of T1DM?

A

Autoimmune against Beta cells - viral infection can trigger autoimmune response
Idiopathic
Genetic susceptibility - HLA-DR3 and HLA-DR4

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28
Q

What are the risk factors for T1DM?

A
  • Family history
  • Associated with OTHER autoimmune disease: thyroidisms, coeliacs, Addison’s, perncious anaemia
  • Viral infection with enteroviruses
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29
Q

How is T1DM treated?

A
  1. insulin – basal bolus
  2. lifestyle advice on carb counting and diet + SICK days
    - Basal bolus regimen = long acting dose OD or BD + rapid acting doses before meals
    - Mixed insulin regimen: short/rapid acting + intermediate acting insulins mixed BD good for pts that don’t like multiple injections. Good for kids.
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30
Q

What are the complications of T1DM treatments?

A

Hypoglycaemia
Lipohypertrophy
Weight gain

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31
Q

What is the aim of T1DM treatment?

A

Aims to keep the blood sugar level as close to normal as possible to delay or prevent complications

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32
Q

What is the acute presentation of diabetes mellitus?

A 
Young people (usually DMT1) often present in first 2-6 weeks with polyuria and nocturia, polydipsia and weight loss 
Patients may have ketonuria and breath smelling of ketones (Pear drops)
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33
Q

What is the subacute presentation of diabetes mellitus?

A

Occurs during first months-years
Typical triad of polyuria, polydipsia and weight loss but all are less marked
Also lack of energy, visual blurring, infections

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34
Q

What are the complications that can be the presenting features for diabetes mellitus?

A
  • Staph. skin infection
  • Retinopathy
  • Polyneuropathy causing tingling and numbness in the feet
  • Erectile dysfunction
  • Arterial disease
  • DKA
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35
Q

What would be the only clinical feature of asymptomatic diabetes mellitus?

A

Glycosuria/hyperglycaemia

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36
Q

What is the plasma glucose concentration that is diagnostic for diabetes mellitus (DMT1 usually)?

A
  • Random plasma glucose >11.1 mmol/L
  • Fasting plasma glucose >7 mmol/L
  • Oral glucose tolerance test: >11mmol/L two hours after a 75g oral glucose load
  • In symptomatic individuals, one result is diagnostic. -
    • If there is only one positive, perform a oral glucose tolerance test (again >7 for fasting, and >11.1 for random)
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37
Q

What test can be performed for diabetes mellitus risk?

A

IGT (Impaired glucose tolerance)

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38
Q

What is the main test for DMT2?

A

HbA1c > 48

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39
Q

What is the epidemiology of hyperosmolar, hyperglycaemic state?

A

Patients present in middle/later life often with previously undiagnosed diabetes

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40
Q

What are the risk factors for hyperosmolar, hyperglycaemic state?

A

Infection= Most common cause
Myocardial infarction
Poor medication compliance

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41
Q

Briefly explain the pathophysiology of hyperosmolar, hyperglycaemic state?

A
  • T2DM causes insulin resistance and relative deficiency -> hyperglycaemia -> osmotic diuresis: glucose loss in the urine and water follows
  • This causes osmotic diuresis and hyperosmolarity -> polyuria, polydipsia, dehydration, confusion etc.
  • Endogenous insulin levels are reduced but are still sufficient to inhibit hepatic ketogenesis but insufficient to inhibit hepatic glucose production
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42
Q

What is the clinical presentation of hyperosmolar, hyperglycaemic state?

A
  • Severe dehydration
  • Decreased consciousness
  • Hyperglycaemia
  • Hyperosmolality
  • No ketones in blood/urine
  • Stupor or coma
  • Bicarbonate isn’t lowered + no acidosis
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43
Q

How is hyperosmolar, hyperglycaemic state diagnosed?

A
  • Urine dipstick – glycosuria no ketones
  • Bedside ketone and capillary glucose: hyperglycaemia ≥11mmol/l without significant ketonemia
  • ABG or VBG = hyperglycaemia without metabolic acidosis
  • Plasma osmolality is extremely high
  • Total body K+ is low, but serum K+ is often raised
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44
Q

How is hyperosmolar, hyperglycaemic state treated?

A

Lower rate of insulin infusion
Fluid replacement with 0.9% saline
Restore electrolyte loss potassium replacement
Low molecular weight heparin (SC Enoxaparin) to reduce risk of thromboembolism, MI, stroke, and arterial thrombosis

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45
Q

What blood glucose level is classed as hypoglycamia?

A
  • Plasma glucose <4 mmol/L
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46
Q

What is the aetiology of hypoglycamia?

A
  • In diabetes= due to insulin or sulphonylurea treatment
  • In non diabetes= Exogenous drugs, pituitary insufficiency, liver failure, Addison’s disease, Islet’s cell tumour, Non pancreatic neoplasm, burns, sepsis
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47
Q

What is the clinical presentation of hypoglycamia?

A
  • Autonomic= Sweating, anxiety, hunger, tremor, palpitations, dizziness
  • Neuroglycopenic= Confusion, drowsiness, visual trouble, seizures, coma
  • Rarely, focal symptoms= Personality change, transient hemiplegia, mutism etc
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48
Q

How is hypoglycamia diagnosed?

A
  • Fingerprick blood glucose= Shows hypoglycaemia,
  • bloods: C peptide and ketones
  • Take drug history and exclude liver failure
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49
Q

How is hypoglycamia treated?

A

Oral sugar and long acting starch

If pt is concsious
- Fast acting carb :Glucose tablets, gel or liquid or fruit juice. Then recheck blood glucoe after 10-15 mins.
- Long acting carb: once BG>4mmol/L – a meal if due or snack like bread or biscuits.
- IM glucagon or IV glucose: given if pt doesn’t respond to the fast acting glucose

If pt is unconscious
- IM glucagon first
- IV glucose: 10% or 20% solution
- Long acting carb: once BG >4mmol/L – a meal if due or snack like bread or biscuits.

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50
Q

What is the epidemiology of diabetic nephropathy?

A

Clinical nephropathy secondary to glomerular disease usually manifests 15-25yrs after diagnosis and affects 25-35% of patients diagnosed under age 30

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51
Q

What is the pathophysiology of diabetic nephropathy?

A

Thickening of the basement membrane in glomerulus due to poor glycaemic control, which leads to micro-albuminuria

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52
Q

What are the risk factors for diabetic nephropathy?

A

Poor blood pressure and blood glucose control

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53
Q

How is diabetic nephropathy diagnosed?

A
  • Urine albumin:creatinine ratio >3 will indicate micro albuminuria
  • This may progress to intermittent albuminuria followed by persistent proteinuria
  • Normochromic normocytic anaemia
  • raised ESR
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54
Q

How is diabetic nephropathy treated?

A
  • Aggressive treatment of high BP
  • Reductions in insulin dosage as insulin sensitivities is increased
  • Avoid drugs excreted via kidney
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55
Q

What is the epidemiology of diabetic neuropathy?

A

Affects 30-35% of patients with diabetes

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56
Q

What is the aetiology of diabetic neuropathy?

A

Isolated mononeuropathies are thought to be as a result of occlusion of the vasa nervorum. More diffuse neuropathies may arise from the accumulation of the fructose and sorbitol which disrupts the structure and function of the nerve

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57
Q

What are the risk factors of diabetic neuropathy?

A

Hypertension, Smoking, HbA1c, BMI

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58
Q

What are the clinical features of diabetic neuropathy?

A
  • Pain: allodynia, burning etc
  • Autonomic: Postural hypotension, gastroparesis, diarrhoea, constipation
  • Insensitivities: Glove and stocking sensory loss
  • Mononeuritis multiplex: damage to at least 2 different areas of the peripheral nervous system
  • Diabetic amyotrophy
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59
Q

How is diabetic neuropathy treated?

A
  • Good glycaemic control
  • Treated with paracetamol
  • Tricyclic antidepressants
  • Anticonvulsants - gabapentin, pregabalin
  • Transcutaneous nerve stimulation
  • Avoidance of weight bearing
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60
Q

What are the most common complications of diabetes?

A
  • macrovascular = Stroke, MI, peripheral vascular disease, IHD, HF
  • Microvascular complications= Diabetic retinopathy, nephropathy, neuropathy
  • Diabetic foot ulceration
  • Infection
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61
Q

What is the epidemiology of diabetic foot ulceration?

A

Foot ulceration occurs in 15% of people with DM

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62
Q

What is the pathophysiology of diabetic foot ulceration?

A
  • Neuropathy results in increased risk of silent trauma of the foot.
  • Furthermore, neuropathy results in autonomic features that results in increased skin dryness of foot, which is thus more susceptible to cracking and ulceration.
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63
Q

What are some preventative methods for diabetic foot ulceration?

A
  • Diabetic foot screening and education
  • Check shoes for sharp bodies
  • Tie shoe laces loosly
  • Keep feet away from heat
64
Q

List some common infections in diabetes?

A
  • UTI
  • Skin infections such as cellulitis, boils, abscesses, staph. infections. Lipohypertrophy
  • Rectal abscess
  • Pyelonephritis
  • Pneumonia
65
Q

List some suggestive features of DMT1 over DMT2?

A
  • DMT1 tends to occur in childhood
  • Acute presentation
  • Tend to be leaner
  • More prone to ketoacidosis
  • High levels of autoantibodies
66
Q

List some suggestive features of DMT2 over DMT1?

A
  • Usually over 30s
  • Onset is gradual
  • Family history
  • Diet and exercise often helps
67
Q

What is the epidemiology of DMT2?

A
  • Very common (incidence increasing)
  • Older, usually over 30
  • More common in men
  • Ethnicity- middle Eastern, SE Asian, Western Pacific
68
Q

What are the causes of DMT2?

A
  • Obesity, lack of exercise, calorie and alcohol excess
  • No HLA disturbance but genetic link
  • Polygenic disorder
69
Q

What are the risk factors for DMT2?

A
  • Age: typically occurs in adults but the incidence amongst children and adolescents is increasing
  • Ethnicity: Asian and African
  • Family history: 75% risk if both parents have T2DM
  • Gestational diabetes
  • Polycystic ovary syndrome
  • Drugs: corticosteroids, thiazide diuretics
  • Obesity and poor exercise
70
Q

Briefly explain the pathophysiology of DMT2

A
  • Insulin resistance caused by repeated exposure to high blood glucose and insulin -> pancreatic beta cell fatigue and ↓ insulin production.
  • Environmental factors - Obesity – and genetics paly a role in development.
71
Q

How is DMT2 treated?

A
  1. Exercise, diet, weight loss, BP and lipid control
  2. Biguanide e.g. metformin (Reduces rate of gluconeogenesis and increases cell sensitivity to insulin)
  3. SGLT2 inhibitors, sulfonylureas, DPP4-inhibitors, GLP-1 agonists, insulin
72
Q

What is Cushing’s syndrome?

A

A general term which refers to chronic excessive and inappropriate elevated levels of circulating cortisol, whatever the cause

73
Q

What is Cushing’s disease?

A

Specifically refers to the excess of glucocorticoids resulting from inappropriate ACTH secretion from the pituitary due to a tumour

74
Q

What is the epidemiology of Cushing’s syndrome?

A
  • 10 per 100,000
  • Higher incidence in diabetics
  • 2/3rds are due to cushing’s disease
75
Q

What is the aetiology of Cushing’s syndrome?

A
  • ACTH dependent causes= Cushings disease, Ectopic ACTH production, ACTH treatments (e.g. for asthma)
  • ACTH independent causes= Adrenal adenoma, iatrogenic e.g. oral glucocorticoids

C–Cushing’s disease (a pituitary adenoma secreting excessiveACTH)
A–Adrenal adenoma (anadrenal tumoursecreting excesscortisol)
P–Paraneoplastic syndrome
E–Exogenous steroids (patients taking long-term corticosteroids)

76
Q

Briefly explain the pathophysiology of Cushing’s syndrome?

A

Excess cortisol from:
- adrenal adenomas or hyperplasia which cause zona reticularis to release cortisol.
- iatrogenic causes e.g. glucocorticoids
- alcohol excess, severe depression, obesity, pregnancy
- pituitary adenoma or ectopic tumour secreting ACTH

77
Q

What is pseudo-Cushings syndrome?

A
  • Cushingoid symptoms + abnormal cortisol levels BUT no HPA pathology associated

causes:
- Alcohol, pregnancy, obesity + severe depression

Will get better after 48 hrs without alcohol

78
Q

What is the clinical presentation of Cushing’s syndrome?

A
  • Proximal weakness and Osteoporosis
  • Plethoric complexion with moon face and acne
  • Mood= Depression, lethargy, irritability, psychosis
  • Obesity= Fat distribution is central (Buffalo hump) with purple striae
  • Muscle atrophy, thick skin that bruises easily
  • Failure for children to grow tall
  • Gonadal dysfunction
  • Infections
  • High BP
  • Hyperglycaemia
79
Q

How is Cushing’s disease diagnosed?

A
  • Drug history to exclude oral steroids
  • Overnight dexamethasone suppression test (No suppression in Cushings
  • Random plasma cortisol (but may be inaccurate)
  • Urine free cortisol over 24hrs
  • **
  • CT/MRI on adrenals
  • Corticotropin releasing hormone test= if cortisol responds, cushings is likely
  • Salivary cortisol
80
Q

How is Cushing’s syndrome treated?

A
  • Iatrogenic= Stop steroids
  • Cushings disease= Surgical selective removal of pituitary adenoma/ bilateral adrenalectomy if source is undetectable
  • Cortisol synthesis inhibition: Metyrapone, ketoconazole
81
Q

What is the clinical presentation of hyperthyroidism?

A
  • Palpitations, tremor and hyperkinesia
  • Diarrhoea, weight loss and increased appetite
  • Olgiomenorrhoea
  • Heat intolerance and sweating
  • Behavioural change= Anxiety and irritability
  • Lid lag and “stare”
  • Proxima myopathy and muscle wasting
  • Hands: Palmar erythma, fine tremor
  • Diffuse goitre
  • Lymphadenopathy and splenomegaly
82
Q

How is hyperthyroidism diagnosed?

A
  • Clinical
  • Thyroid function tests- low TSH, High T4/3
  • Will be raised TSH in secondary hyperthyroidism
  • TPO and thyroglobulin antibodies
  • Ultrasound of thyroid
  • TSH receptor stimulating antibodies are raised (Diagnostic of graves)
83
Q

How is hyperthyroidism treated?

A
  • Antithyroid drugs = Propylthiouracil (Stops conversion of T4 to T3) or Oral carbimazole (Blocks thyroid hormone biosynthesis and immunosuppressant)
  • This can be done via titration or block-replace therapy
  • Radioactive iodine
  • Surgery
84
Q

What are the causes of hyperthyroidism?

A
  • Graves’ (most common)
  • Toxic multinodular goitre
  • Solitary toxic adenoma
  • Drug induced hyperthyroidism - amiodarone
  • De Quervain’s thyroiditis
85
Q

What is the epidemiology of Hashimoto’s thyroiditis?

A
  • Much more common in women

- Most common cause of goitrous hypothyroidism

86
Q

What are the clinical features of Hashimoto’s thyroiditis?

A
  • Thyroid gland may enlarge rapidly, occasionally with dyspnoea or dysphagia from pressure on neck= nodular goitre
    • Hashimoto’s thyroiditis can initially cause a goitre, after which there is atrophy (wasting) of the thyroid gland.
  • Hypothyroidism= Fatigue, cold intolerance, slowed movement, decreased sweating, hyporeflexia, heavy periods, bradycardia, weight gain, constipation,
87
Q

Briefly explain the pathophysiology of Hashimoto’s thyroiditis

A

an autoimmune condition where antithyroid antibodies that attack the thyroid tissue, causing progressive fibrosis -> Inadequate thyroid hormone production and secretion

88
Q

How is Hashimoto’s thyroiditis diagnosed?

A
  • TSH levels raised
  • low T3, T4
  • Anti-TPO 95%

- Thyroid antibodies
- Anti-TPO 95%
- anti-thyroglobulin 50%

89
Q

How is Hashimoto’s thyroiditis treated?

A
  • Thyroid hormone replacement (levothyroxine)

- Resection of obstructive goitre

90
Q

What are the complications of Hashimoto’s thyroiditis?

A
  • Hyperlipidaemia and IHD
91
Q

What is the aetiology of secondary hypoadrenalism ?

A
  • Inadequate adrenocorticotropic hormone (ACTH) and a lack of stimulation of the adrenal glands, leading to low cortisol.
  • This is the result of loss or damage to the pituitary gland: e.g. trauma, tumours, surgery.
92
Q

Briefly explain the pathophysiology of secondary hypoadrenalism

A

Reduction in the release of ACTH from the anterior pituitary gland results in decreased glucocorticoid (cortisol)

93
Q

What is the clinical presentation of secondary hypoadrenalism?

A
  • Patient may have vague symptoms of feeling unwell
  • fatigue, weakness, weight loss, nausea, vomiting, and diarrhea

- No skin hyperpigmentation since ACTH is reduced

94
Q

How is secondary hypoadrenalism diagnosed?

A

ACTH levels are low + low cortisol

Mineralocorticoid production is intact

95
Q

How is secondary hypoadrenalism treated?

A
  • Oral hydrocortisone
  • IV if acute
96
Q

What are the risk factors for diabetic retinopathy?

A
  • Long duration DM
  • Poor glycaemic control
  • Hypertensive
  • On insulin treatment
  • Pregnancy
97
Q

How will proliferative retinopathy be seen?

A
  • New vessels on disc and elsewhere
  • Pre retinal or vitreous haemorrhage
  • Fibrous +/- tractional retinal detachment
98
Q

How is diabetic retinopathy treated?

A
  • Laser therapy = stabilises deterioration and prevents progression (doesn’t cure)
99
Q

How is diabetic retinopathy usually diagnosed?

A
  • National eye screening programme with retinal photography
100
Q

What is the epidemiology of diabetic ketoacidosis?

A
  • Hallmark of DMT1

- Usually can’t occur in DMT2 unless very advanced

101
Q

What are the clinical features of diabetic ketoacidosis?

A
  • The excess ketones are excreted in the urine and appear in the breath= pear drop scent
  • Profound dehydration and vomitting= eyes are sunken, tissue turgor is reduced and tongue is dry
    • polydipsia +polyuria
    • can lead to shock in severe cases
  • Gradual drowsiness, lethargy + confusion.
  • May have severe abdominal pain
  • Kussmaul’s respiration (Deep and rapid)
  • Body temp is often subnormal
102
Q

What are the risk factors for diabetic ketoacidosis?

A
  • Stopping insulin therapy
  • Infection e.g. UTI
  • Surgery
  • MI
  • Pancreatitis
  • Undiagnosed diabetes
103
Q

How is diabetic ketoacidosis diagnosed?

A
  • Blood glucose>11mmol/l
  • Plasma ketones >3mmol/L
  • Acidaemia, blood pH <7.3
  • Bicarbonate <15mmol/L
  • Urine dipstick= Glycosuria and ketonuria
  • Total body K+ is low
  • Increased urea and creatinine due to dehydration
104
Q

How is diabetic ketoacidosis treated?

A

F – Fluids – IV fluid resuscitation with normal saline (e.g., 1 litre in the first hour, followed by 1 litre every 2 hours)
I – Insulin – fixed rate insulin infusion (e.g., Actrapid at 0.1 units/kg/hour)
G – Glucose – closely monitor blood glucose and add a glucose infusion when it is less than 14 mmol/L
P – Potassium – add potassium to IV fluids and monitor closely (e.g., every hour initially)
I – Infection – treat underlying triggers such as infection
C – Chart fluid balance
K – Ketones – monitor blood ketones, pH and bicarbonate

105
Q

Briefly explain the pathophysiology of diabetic ketoacidosis

A
  • High hepatic gluconeogenesis and peripheral uptake by tissues is reduced
  • High circulating glucose levels result in an osmotic diuresis by the kidneys and consequent dehydration and loss of electrolytes
  • Peripheral lipolysis leading to an increase in circulating FFAs, which are broken down into ketone bodys within the mitochondria
  • Metabolic acidosis then occurs
  • As pH falls, pH dependant enzyme systems can’t function
106
Q

What is the epidemiology of Addison’s disease?

A
  • Very rare= 0.8 per 100,000

- Marked female preponderance

107
Q

What are the common causes of Addison’s disease?

A
  • Autoimmune adrenalitis
  • TB, meningococcal infection
  • Adrenal metastases
  • Opportunistic infections in HIV
108
Q

Briefly explain the pathophysiology of Addison’s disease

A
  • Destruction of the entire adrenal cortex
  • Reduced glucocorticoid, mineralocorticoid and androgen production
  • Increased CRH, and ACTH in response to low cortisol levels
109
Q

What is the clinical presentation of Addison’s disease?

A
  • Lethargy
  • Low mood, Low self esteem
  • Anorexia and weight loss
  • Vitiligo, tanned skin, pigmentation of skin
  • Vomitting and nausea
  • Diarrhoea, constipation and abdominal pain
  • Amenorrhoea
  • Postural hypotension, dizziness
  • Lean build
  • Dehydration, critical deterioration
110
Q

How is Addison’s disease diagnosed?

A
  • Blood tests: Hyponatraemia, hyperkalaemia, hypoglycaemia, hypoaldosteronism, low cortisol, uraemia, Raised Ca2+, FBC, Eosinophilia
  • Short ACTH stimulation test= Measure cortisol 30mins after IM tetracosactide. Exclude Addisons if cortisol >550nmol/L
  • Adrenal antibodies = Adrenalitis
  • 9am ACTH. If increased= Addison’s
111
Q

How is Addison’s disease treated?

A
  • If patient is seriously ill= IV hydrocortisone, IV 0.9% saline, glucose infusion if hypoglycaemia
  • Replace steroids x3 daily= Glucocorticoids (oral hydrocortisone) and mineralocorticoids (oral fludrocortisone)
  • Increase steroids in stress, illness, pregnancy
112
Q

What are the clinical features of an Adrenal crisis?

A
  • Vomitting and nausea
  • Abdominal pain
  • Muscle cramps
  • Confusion
113
Q

How is an Adrenal crisis treated?

A
  • IV hydrocortisone immediately
114
Q

What is the epidemiology of hypocalcaemia?

A
  • Very common in hospitalised patients

- Correlates with severity of illness

115
Q

What is the clinical presentation of hypoparathyroidism/hypocalcaemia?

A

SPASMODIC= Spasms (Tetany), Paresthesia, Anxiety, Seizures, Muscle tone increased (wheeze), Orientation impaired, Dermatitis and diarrhoea, Cataracts, Chvostek’s sign and cardiomyopathy

116
Q

What are the causes of hypocalcaemia?

A
  • Chronic kidney disease
  • Severe vitamin D deficiency
  • Reduced PTH function= hypoparathyroidism, pseudohypoparathyroidism, pseudopseudohypoparathyroidism
117
Q

What are the clinical features of pseudohypoparathyroidism?

A
  • Short stature
  • Short metacarpals (4th)
  • Subcutaneous calcification
  • May be intellectual impairment
118
Q

What are the results of a pseudohypoparathyroidism serum blood test?

A
  • High serum PTH
  • Low serum Ca2+
  • High serum phosphate
119
Q

How is hypocalcaemia diagnosed?

A
  • Blood tests= Ca2+, PTH, PO4
  • X ray of metacarpals for pseudohypoparathyroidism
  • Serum urea, creatinine and eGFR for renal function
  • Parathyroid antibodies in idiopathic hypoparathyroidism
  • Vit D and magnesium levels
  • ECG= QT elongation in hypocalcaemia
120
Q

What are the results of a hypoparathyroidism serum blood test?

A
  • Low serum Ca2+
  • Low serum PTH
  • High serum PO4
121
Q

What are the results of a pseudopseudohypoparathyroidism serum blood test?

A
  • Normal serum Ca2+
  • Normal serum PTH
  • Normal serum PO4
122
Q

How is hypocalcaemia/hypoparathyroidism treated?

A
  • IV calcium gluconate over 30 mins with ECG monitoring
  • If vit D defiency= Oral cholecalciferol or oral adcal
  • Hypoparathyroidism= Calcium supplements and calcitriol
123
Q

What is the epidemiology of Graves’ disease?

A
  • More common in females

- Most commonly presents at 40-60 yrs

124
Q

What are the risk factors for Graves’ disease?

A
  • Female
  • Genetic- HLA B8, DR3, DR2
  • E coli and other gram negative bacteria
  • Smoking
  • Stress
  • High iodine intake
  • Autoimmune disease= Vitiligo, DMT1, Addiso’s etc
125
Q

Briefly explain the pathophysiology of Graves’ disease

A
  • Thyroid stimulating immunoglobulins recognise and bind to immunoglobulins recognise and bind to the TSH receptor which stimulates T3/4
  • Thyroxine receptors in the pituitary are activated by excess hormone
  • Therefore reduced release of TSH in negative feedback loop, so high levels of T3/4 and low TSH
126
Q

What are the specific clinical features of Graves’ disease?

A
  • Graves ophthalmopathy= Presents in most Graves’ and some autoimmune hypothyroidism patients. Includes retro-orbital inflammation, eye discomfort, conjunctival oedema, photophobia, reduced acuity
  • Graves dermopathy= Pretibial myxoedema, and swollen clubbed fingers
127
Q

What is the epidemiology of thyroid carcinoma?

A
  • Not common

- More common in females

128
Q

What are the types of thyroid carcinoma?

A
  • Papillary (70%)
  • Follicular (20%)
  • Anaplastic (<5%)
  • Lymphoma (2%)
  • Medullary cell (5%)
129
Q

What is the most common type of thyroid carcinoma?

A

Papillary (70%)

130
Q

What are the clinical features of thyroid carcinoma?

A
  • Thyroid nodules
  • Thyroid may increase in size, and be hard and irregular
  • May have dysphagia or hoarseness of voice due to tumour compression
131
Q

How is thyroid carcinoma diagnosed?

A
  • Fine needle aspiration cytology biopsy and ultrasound: distinguish between benign and malignant
  • Blood tests (TFTs): To check if hyper or hypo thyroid
132
Q

How is thyroid carcinoma treated?

A
  • Radioactive iodine
  • Levothyroxine to keep TSH reduced
  • Chemotherapy to reduce risk of spread and treat micrometastases
  • Thyroidectomy
133
Q

What is the aetiology of nephrogenic diabetes insipidus?

A
  • Hypokalaemia
  • Hypercalcaemia
  • Drugs: Lithium chloride, glibenclamide
  • Renal tubular acidosis
  • Sickle cell disease
  • Prolonged polyuria of any cause
  • Familial
134
Q

What are the clinical features of diabetes insipidus?

A
  • Polyuria
  • Compensatory polydipsia
  • Hypernatraemia due to water loss in excess of Na+ loss: lethargy, thirst, weakness
  • Can lead to severe dehydration if the thirst mechanism or consciousness is impaired or patient is denied fluid
135
Q

How is diabetes insipidus diagnosed?

A
  • Urine vol to confirm polyuria
  • Check blood glucose to exclude DM
  • Water deprivation test
  • To differentiate between neurogenic or cranial- give IM desmopressin. Urine will not be concentrated in nephrogenic, but will in cranial
136
Q

How is nephrogenic diabetes insipidus treated?

A
  • Treat the cause- usually renal disease
  • Give thiazide diuretics
  • NSAIDs
137
Q

What is the aetiology of cranial diabetes insipidus?

A
  • Idiopathic
  • Congenital defects in ADH gene
  • Diseases of the hypothalamus
  • Tumour
  • Trauma
138
Q

How is cranial diabetes insipidus treated?

A
  • Find the cause- MRI of head and test ant. pituitary

- Give synthetic analogue of ADH e.g. oral desmopressin

139
Q

What is the aetiology of hypokalaemia?

A
  • Increased renal excretion= Diuretics (most common), increased aldosterone, renal disease, mineralocorticoids
  • Reduced dietary K+ intake
  • Redistribution into cells
  • GI losses
140
Q

What are the clinical features of hypokalaemia?

A
  • Usually asymptomatic
  • Muscle weakness
  • Cramps
  • Hypotonia
  • Hyporeflexia
  • Tetany
  • Palpitations
  • Light headedness
  • Constipation
141
Q

How is hypokalaemia diagnosed?

A
  • Serum K+ (less than 3.5= hypokalaemia, less than 2.5. is an emergency)
  • ECG= Small or inverted T waves, prominent U waves, a long PR interval, depressed ST segment
142
Q

How is hypokalaemia treated?

A
  • Medication review (withdrawal from diuretics)
  • Give oral K+ supprlements
  • Can give IV K+ but with extreme caution
143
Q

What is the aetiology of hyperkalaemia?

A
  • Decreased exertion= AKI or oliguric renal failure, Some medications, Addisons
  • Diabetic ketoacidosis
  • Metabolic acidosis
  • Tissue lysis/ necrosis
144
Q

What are the clinical features of hyperkalaemia?

A
  • Asymptomatic until K+ is high enough to cause cardiac arrest
  • Fast irregular pulse, chest pain, dizziness
  • Muscle weakness and fatigue
  • May be associated with metabolic acidosis = kussmauls respiration
145
Q

How is hyperkalaemia treated?

A
  • Medication review
  • Dietary K+ restriction
  • Polystyrene sulfonate resin
  • If urgent, calcium gluconate to stabilise cardiac membrane, and soluble insulin to drive K+ into cells
146
Q

How is hyperkalaemia diagnosed?

A
  • Serum K+. Over 5.5 is hyperkaelaemia, and over 6.5 is emergency
  • Progressive abnormalities on ECG= Tall tented T waves, small P waves, Wide QRS complex
147
Q

What are the clinical features of carcinoid syndrome?

A
  • Diarrhoea
  • Flushing
  • Palpitations
  • Abdominal cramps
  • Signs of right heart failure
  • Bronchospasm
148
Q

How is carcinoid syndrome diagnosed?

A
  • High vol of 5-hydroxyindolaecetic acid
  • Metabolic panel and LFTs
  • Liver ultrasound to confirm metastases
149
Q

How is carcinoid syndrome treated?

A
  • Local disease: Surgical resection and perioperative octreotide infusion
  • Metastases: above and additional radiotherapy ablation
150
Q

What is phaeochromocytoma?

A

A very rare adrenal medullary tumour that secretes catecholamines

151
Q

What are the clinical features of phaeochromocytoma?

A
  • Headache
  • Profuse sweating
  • Palpitations
  • Hypertension
  • Postural hypotension
  • Tremor
  • Hypertensive retinopathy
  • Pallor
152
Q

How is phaeochromocytoma diagnosed?

A
  • Plasma metanephrines and normatanephrines
  • 24 hr urinary total catecholamines
  • CT for tumour
153
Q

How is phaeochromocytoma treated?

A

Alpha blockers
Antihypertensive crisis
Tumour removal

154
Q

What would raised TSH receptor stimulating antibodies be indicative of?

A

Graves’ disease

155
Q

What would TPO and thyroglobulin antibodies be indicative of?

A

Graves or other causes of hyperthyroidism

156
Q

What are the clinical features of hypothyroidism?

A
  • Cold intolerance
  • Low mood
  • Fatigue
  • Constipation
  • Weight gain
  • Decreased sweating
  • Amenorrhea
157
Q

what is kussamaul breathing

A

deep, laboured breathing associated with metabolic acidosis = compensatory mech to reduce acidity

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